In the spinal cord of the unanesthetized cat stimulation of large cutaneous afferents reduces the excitability of Ia afferent terminals within the motor nucleus. This effect is assumed to be due to primary afferent hyperpolarization (PAH) and is associated with increased amplitude of the Ia monosynaptic EPSPs of extensor motoneurons. Evidence is provided that in many cases the Ia EPSP enhancement produced by cutaneous conditioning, as well as the Ia EPSP depression produced by stimulation of group I fibers of flexor muscles is of presynaptic origin. Cutaneous conditioning also reduced the excitablity fluctuations and the correlation between excitability fluctuations of independent sets of Ia afferent terminals, as well as the correlated fluctuations of the Ia EPSPs recorded from pairs of gastrocnemius motoneurons, often without changing the mean Ia EPSPs. These observations suggest that in addition to the stochastic mechanism responsible for transmitter release at each presynaptic terminal there is another mechanism causing correlated transmitter release of many Ia afferent terminals. Such a mechanism seems to result from activity in the segmental pathways responsible for PAD, and provides a way for controlling the information transmitted from Ia fibers to motoneurons.